Cheaper, Simpler, and Better: Tips for Treating Seniors With Parkinson Disease

Ahlskog, J. Eric

doi:10.4016/37075.01

Cited by 5 publications

(4 citation statements)

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“…Levodopa is believed to compete with other neutral AAs for its active transport across the BBB, as well as across small intestine enterocytes. In the brain, levodopa has been suggested to be transported by the neutral AA heterodimeric transporter LAT1-4F2hc (SLC7A5-SLC3A2) (Uchino et al, 2002;Morimoto et al, 2008;Ahlskog, 2011). Intestinal levodopa transport has also been suggested to be mediated by neutral AA transporters (Lennernas et al, 1993), but the identity of the transporters involved in its intestinal absorption is still unknown.…”

Section: Introductionmentioning

confidence: 99%

“…Parkinson's disease (PD) is a neurodegenerative disorder mainly caused by dopamine depletion in the substantia nigra, clinically manifested by symptoms including its hallmark, the trias of bradykinesia, resting tremor, and rigidity (Nyholm and Lennernas, 2008;Ahlskog, 2011;Hickey and Stacy, 2011). Since its introduction in 1968, levodopa (L-dihydroxyphenylalanine, L-DOPA) is the major therapeutic agent in treating PD (Poewe et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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The Molecular Mechanism of Intestinal Levodopa Absorption and Its Possible Implications for the Treatment of Parkinson’s Disease

Camargo

Vuille‐dit‐Bille

Mariotta

et al. 2014

J Pharmacol Exp Ther

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Levodopa (L-DOPA) is the naturally occurring precursor amino acid for dopamine and the main therapeutic agent for neurologic disorders due to dopamine depletion, such as Parkinson's disease. L-DOPA absorption in small intestine has been suggested to be mediated by the large neutral amino acids transport machinery, but the identity of the involved transporters is unknown. Clinically, coadministration of L-DOPA and dietary amino acids is avoided to decrease competition for transport in intestine and at the bloodbrain barrier. L-DOPA is routinely coadministered with levodopa metabolism inhibitors (dopa-decarboxylase and cathechol-O-methyl transferase inhibitors) that share structural similarity with levodopa. In this systematic study involving Xenopus laevis oocytes and Madin-Darby canine kidney epithelia expression systems and ex vivo preparations from wild-type and knockout mice, we identified the neutral and dibasic amino acids exchanger (antiporter) AT-rBAT substrates, whereas dopadecarboxylase and cathechol-O-methyl transferase inhibitors had no effect. The presence of amino acids in the basolateral compartment mimicking the postprandial phase increased transepithelial levodopa transport by stimulating basolateral efflux via the antiporter LAT2-4F2 (SLC7A8-SLC3A2). Additionally, the aromatic amino acid uniporter TAT1 (SLC16A10) was shown to play a major role in L-DOPA efflux from intestinal enterocytes. These results identify the molecular mechanisms mediating small intestinal levodopa absorption and suggest strategies for optimization of delivery and absorption of this important prodrug.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Molecular Mechanism of Intestinal Levodopa Absorption and Its Possible Implications for the Treatment of Parkinson’s Disease

Camargo

Vuille‐dit‐Bille

Mariotta

et al. 2014

J Pharmacol Exp Ther

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“…A detailed discussion of how to initiate and dose carbidopa/levodopa is beyond the scope of this writing but can be found in an article published nearly a decade ago. 64 A more extensive PD treatment text has been published since and remains appropriate for current needs. 1…”

Section: The New Millennium: Clinicians Still Advised To Spare Levodopamentioning

confidence: 99%

Common Myths and Misconceptions That Sidetrack Parkinson Disease Treatment, to the Detriment of Patients

Ahlskog

2020

Mayo Clinic Proceedings

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Parkinson disease symptoms become apparent when there has been substantial loss of brain dopamine. That is the consequence of the slow progression of the Lewy body neurodegenerative process. Replenishment of brain dopamine with levodopa therapy dates back approximately a half century and continues to be the most efficacious symptomatic treatment. Understanding the fundamentals of levodopa treatment is crucial to therapeutic success. Various myths over the years have sabotaged treatment outcomes and have discouraged primary care physicians from managing patients with Parkinson disease. That is unfortunate because in some regions, neurologists, and in particular movement specialists, are in short supply. The long history of these persistent levodopa myths and the counterarguments are the focus of this article.

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“…18 Estos medicamentos reducen el riesgo de la discinesia y las fluctuaciones motoras en las etapas tempranas de la enfermedad y en aquellos pacientes cuyas manifestaciones se iniciaron antes de los 40 años de edad.…”

Section: Tratamientounclassified

La enfermedad de Parkinson: neurología para psiquiatras

2013

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SUMMARYParkinson's disease is a progressive and degenerative disease due to the loss of the substantia nigra dopaminergic neurons in the mesencephalon. Its manifestations are: tremor at rest, rigidity and slowing of movements, and alterations in posture and gait. The early onset of dementia or the presence of hallucinations, not related to the dopaminergic treatment, are associated with the presence of dementia with Lewy bodies (DLB) or Alzheimer's disease. The scales used to assess the stage and severity of Parkinson's disease are: the scale of Stages of Hoehn and Yahr, and the Unified Parkinson's Disease Rating Scale. Although there is not a drug that stops the progression of Parkinson's disease, the current treatment for this illness consist in: a) dopamine replacement through the use of its precursor, levodopa, b) administering substances, like ropinirole, pramipexole, and bromocriptine, that increase dopamine activity to stimulate their receptors, and c) inhibiting the enzymes that destroy dopamine as the catechol-O-methyltransferase with entacapone, and monoamine oxidase type B (MAO B ) with selegiline and rasagiline. Surgical treatment of Parkinson's disease consists of ablative procedures and deep brain stimulation. This review describes their indications, administration and side effects. RESUMENLa enfermedad de Parkinson es una enfermedad degenerativa y progresiva debida a la pérdida de las neuronas dopaminérgicas de la sustancia nigra del mesencéfalo. Sus manifestaciones son: temblor en reposo, rigidez y enlentecimiento de los movimientos, alteraciones en la postura y en la marcha. La aparición temprana de problemas en la memoria o alucinaciones, no debidas al tratamiento, indica la presencia de demencia con cuerpos de Lewy. Las escalas utilizadas para evaluar el estadio y la gravedad de la enfermedad de Parkinson son: la Escala de los Estadios de Hoehn y Yahr y la Escala Unificada de Calificación de la Enfermedad de Parkinson (UPDRS). Aunque todavía no existe un medicamento que detenga la evolución de la enfermedad de Parkinson, el tratamiento actual consiste en mejorar los síntomas mediante: a) la reposición de la dopamina por medio del uso de su precursor (levodopa, L-Dopa), b) la administración de sustancias que aumentan la actividad dopaminérgica al estimular a sus receptores (ropinirol, pramipexol, bromocriptina) y c) la inhibición de las enzimas que destruyen la dopamina como la catecol-O-metiltransferasa (COMT) con la entacapona, y a la monoamino oxidasa tipo B (MAO B ) con la selegilina y la rasagilina. Existe además el tratamiento quirúr-gico de la enfermedad de Parkinson que consiste en procedimientos ablativos y la estimulación cerebral profunda. En esta revisión se describen los elementos básicos de la enfermedad, su cuadro clínico y sus complicaciones. En una segunda parte se aborda el tratamiento médico con sus indicaciones, administración y efectos secundarios, y para terminar se describirá el tratamiento quirúrgico.Palabras clave: Enfermedad de Parkinson, antiparkinsónicos, cuadro clí...

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Cheaper, Simpler, and Better: Tips for Treating Seniors With Parkinson Disease

Cited by 5 publications

References 17 publications

The Molecular Mechanism of Intestinal Levodopa Absorption and Its Possible Implications for the Treatment of Parkinson’s Disease

The Molecular Mechanism of Intestinal Levodopa Absorption and Its Possible Implications for the Treatment of Parkinson’s Disease

Common Myths and Misconceptions That Sidetrack Parkinson Disease Treatment, to the Detriment of Patients

La enfermedad de Parkinson: neurología para psiquiatras

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